Our research involves studying the hypothetical role of oncogene activation by translocation to functionally active immunoglobulin gene regions in the genesis of murine plasmacytoma (MCP) and human Burkitt's lymphoma (BL). We will attempt to determine the location of the immunoglobulin genes in relation to the translocation breakpoints, and to prove the existence of the postulated oncogenes. We also will be continuing cytogenic studies on human Burkitt's lymphoma and related conditions. Cytogenic studies on mouse and rat plasmacytomas are being conducted to discover (1) if the specific translocations associated with BALB/c plasmacytomas are also identifiable in plasmacytomas of another, unrelated mouse strain; (2) whether the functionally active or inactive chromosomes 12 and 6, respectively, serve as the recipient of the distal fragment of chromosome 15 in the plasmacytoma-associated translocation; (3) whether the genetic content of the distal fragment of chromosome 15 plays a direct role in the genesis of plasmacytomas; (4) what role the plasmacytoma-associated translocation and deletion chromosomes play in determining tumorigenic behavior by somatic hydridization; (5) how chromosome 12 is involved in plasmacytogenesis; (6) if the plasmacytoma-associated translocations are accompanied by any morphological and/or staining differences in the banding pattern of the translocated segment. Continued cytogenic studies on murine leukemia will include an analysis of the leukemia-related genetic polymorphism of chromosome 15; pilot studies with isolated chromosome 15, duplicated in the course of T cell leukogenesis; somatic hybrid studies on the antagonistic influence of leukemia-derived versus normal parent cell-derived chromosomes 15 on the expression of the tumorigenic phenotype; and comparative lymphoma/plasmacytoma studies.